Abstract：Objective: To investigate the effect of atractylenolide I (ATR-I) on inflammatory response in acute myocardial infarction (AMI) rats. Methods: The rats were divided into a sham operation group, an AMI group, an ATR-Ⅰ-L dose group, an ATR-Ⅰ-M dose group, an ATR-Ⅰ-H dose group, and an ATR-Ⅰ-H + plerixafor (AMD3100) model group, with 12 rats in each group, once a day for 7 days.The ultrasound imaging system was applied to measure fraction shorting (FS) and left ventricular ejection fraction (LVEF) in rats. The myocardial infarction area, myocardial histopathology, and cardiomyocyte apoptosis in rats were detected by 2,3,5-triphenyl tetrazolium chloride (TTC) staining, hematoxylin-eosin (HE) staining, and terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, respectively. The changes in lactate dehydrogenase (LDH), myoglobin (MB), interleukin-1β (IL-1β), and tumor necrosis factor-α (TNF-α) in myocardial tissue were calculated by enzyme-linked immunosorbent assay (ELISA). Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) and Western blot were employed to determine the expression levels of stromal cell-derived factor 1( SDF-1 )and C-X-C chemokine receptor type 4(CXCR4), and the proteins expression of SDF-1 and CXCR4 mRNA in rat tissues. Results: Compared with the sham surgery group, the levels of LVSF and FS, and the expression of SDF-1, CXCR4 mRNA and their protein expression in myocardial tissue of AMI group decreased significantly (P<0.05). The myocardial infarction area, apoptosis rate, and levels of LDH activities, MB, IL-1β, and TNF-α in myocardial tissue increased significantly (P<0.05), with severe myocardial cell damage and inflammation. Compared with the AMI group, the levels of LVSF and FS, and the expression of SDF-1, CXCR4 mRNA and their protein expression in myocardial tissue of ATR-I-L group, ATR-I-M group, and ATR-I-H group increased significantly (P<0.05). The myocardial infarction area, apoptosis rate, and levels of LDH activities, MB, IL-1β, and TNF-α in myocardial tissue decreased significantly (P<0.05), the myocardial cell damage had improved. Compared with the ATR-I-H group, the LVSF and FS, and the expression of SDF-1, CXCR4 mRNA and their protein expression in myocardial tissue of ATR-I-H+AMD3100 group decreased significantly (P<0.05), the myocardial infarction area, apoptosis rate, and levels of LDH activities, MB, IL-1β, and TNF-α in myocardial tissue increased significantly(P<0.05), the damage to myocardial cells intensified. Conclusion: ATR-I can reduce inflammation in AMI rats.
[1] 钟金鹏,杨莉,王辉波,等.HMGB1减弱丹参酮ⅡA对大鼠心肌缺血/再灌注损伤的缓解作用[J].基础医学与临床,2022,42(9):1333-1338. [2] Sun C,Zhang X,Yu F,et al.Atractylenolide I alleviates ischemia/reperfusion injury by preserving mitochondrial function and inhibiting caspase-3 activity[J].Int Med Res,2021,49(2):315-337. [3] 宋雪梅,秦合伟,李彦杰,等.基于miR-381调控SDF-1/CXCR4信号通路探讨电针对缺血性脑卒中后神经损伤修复的影响[J].中国针灸,2024,44(2):175-181. [4] 李文彬,郑祥德,吴昌徽,等.血清CXCL12、SDF-1α、CXCR4水平与颅脑损伤患者预后的相关性[J].分子诊断与治疗杂志,2020,12(12):1749-1752. [5] Matter MA,Paneni F,Libby P.Inflammation in acute myocardial infarction:the good,the bad and the ugly[J].Eur Heart,2024,45(2):89-103. [6] Gupta L,Thomas J,Ravichandran R,et al.Inflammation in cardiovascular disease:a comprehensive review of biomarkers and therapeutic targets[J].Cureus,2023,15(9):45483-45499. [7] Sadri F,Rezaei Z,Fereidouni M.The significance of the SDF-1/CXCR4 signaling pathway in the normal development[J].Mol Biol Rep,2022,49(4):3307-3320. [8] Otaka F,Ito Y,Nakamoto S,et al.Macrophages contribute to liver repair after monocrotaline-induced liver injury via SDF-1/CXCR4[J].Exp Ther Med,2021,22(1):668-690. [9] 郭静,杨举红,张琳,等.黄芩苷调节SDF-1/CXCR4信号通路对高糖诱导的心肌细胞凋亡的影响[J].河北医学,2024,30(11):1792-1797.
2025, Vol. 31 
冀公网安备13080202000786号